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Mechanisms of Microbial Disease > Chapter 17 > Flashcards

Chapter 17 Flashcards

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1
Q

What is a true food poisoning?

A

Ingestion of a pre-formed toxin (no organism needed)
Faster acting (hours)
Survive cooking/heating

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2
Q

What is a food-associated infection?

A

Food is a vehicle for a pathogen

Slower onset of symptoms

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3
Q

How can a pathogen change fluid balance to cause GI disease?

A

Change the balance of water and electrolytes in the small bowel causing massive fluid secretion

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4
Q

How do cell destruction and inflammation occur to cause GI disease?

A

Invasion and/or cytotoxin production

Will lead to a fever

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5
Q

How does invasion cause GI disease?

A

Penetrates intestinal mucosa allowing the pathogen to spread and multiply outside of the bowel
Blood or pus found in feces

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6
Q

What is diarrhea?

A

The most common outcome of GI tract infections that increases fluid and electrolyte loss in the gut lumen (unformed or liquid faeces)

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7
Q

What does diarrhea allow?

A

Allows the host to get rid of the pathogen and the pathogen to disseminate

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8
Q

How does diarrhea differ in resource-rich and resource poor region?

A

Poor: Major cause of mortality in children
Rich: Usually mild and self-limiting except in very young, elderly and immunocompromised

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9
Q

How do we determine the cause of the diarrhea?

A

Generally difficult to identify based solely on symptoms (important in outbreaks)
Get patient history (food intake, travel)
Macroscopic and microscopic examination of feces for blood and pus

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10
Q

What is a common bacterial cause of diarrhea?

A

E. coli, most versatile, member of gut flora

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11
Q

What does Enteropathogenic E. coli (EPEC) cause?

A

Sporadic cases and outbreak of diarrhea in babies and young children
No toxin production

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12
Q

What are the virulence factors of EPEC?

A

Adhesions, bundle-forming pili and intimin to attach to epithelial cells and microvillus

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13
Q

What does Enterotoxigenic E. coli (ETEC) cause?

A

Most important cause of bacterial diarrhea in children

Presence of E. coli not necessarily important, plasmid is (Need lots to cause problems)

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14
Q

How does ETEC work?

A

Binds to receptors on the cell membrane of the small intestine and produces plasma encoded toxins (heat labile and stable)

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15
Q

How do the 2 plasmid encoded toxins of ETEC work?

A 
Heat labile (LT) toxin increases cAMP, similar mode of action to cholera
Heat stable (ST) toxin increases guanylate cyclase activity which increase cGMP and fluid secretion
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16
Q

Where is Enterohaemorrhagic E.coli (EHEC) found?

A

In the intestine of healthy cattle (uncooked ground beef, unpasteurized milk/juices, contaminated water, bean sprouts, celery)
“Hamburger disease”

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17
Q

How does EHEC work?

A

Invasive and makes toxins that damage the large intestine by inhibiting protein synthesis
Verotoxin I and II (VTEC) or “Shiga like toxin” (SLT-1 and SLT-2)

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18
Q

What are some symptoms of EHEC?

A

Ulceration and bleeding of the large intestine causing bloody diarrhea
Destruction of RBC cause anemia (fatigue, weakness)
Low platelet count and sudden kidney damage

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19
Q

What is the ID50 of EHEC?

A

Very small, only takes a few to cause problems

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20
Q

What is the serotype of EHEC?

A

Serotype O157:H7

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21
Q

What are some complications of EHEC?

A 
Hemorrhagic colitis (destruction of mucosa leading to hemorrhage and bloody diarrhea)
Hemolytic ureic syndrome (HUS-toxin in blood stream)
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22
Q

What may account for the kidney damage by EHEC?

A

Verotoxin receptors found on the renal epithelium

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23
Q

How does Enteroinvasive E. coli (EIEC) work?

A

Attach to the mucosa of the large intestine, invade the cells via endocytosis, multiply, spread to adjacent cells and cause tissue destruction, inflammation and ulceration

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24
Q

What are the symptoms of EIEC?

A

Blood and mucous in the stool

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25
How does enteroaggregative E. coli (EAEC) work?
Aggregation using plasmid-encoded fimbria | Toxins produced but role uncertain
26
How does EAEC appear on tissue culture cells?
Like stacked bricks
27
What does Diffuse-aggregative E.coli (DAEC) produce?
alpha-hemolysin and cytotoxic necrotizing factor | Role in diarrhea not well understood
28
How do we ID EHEC strain?
By probing for shiga toxin genes or proteins (use antibodies-ELISA)
29
How do we ID EIEC strain?
Look for the invasion of tissue culture cells or the presence of invasion associated genes
30
How do we treat diarrhea?
No antibiotics as this can cause more toxin to be released | Fluid and electrolyte replacement and prevention (clean water, pasteurization, proper cooking)
31
Why are antidiarrheal medications (immodium) bad?
Desensitizes the intestinal epithelium to the toxin, increasing the contact time with the intestinal wall which can increase disease severity
32
How do we treat HUS?
Urgent treatment with dialysis
33
What does Salmonella spp cause?
Gastroenteritis, food poisoning and enteric fever (S. typhi makes typhoid fever)
34
Where does salmonella spp. come from?
Meat, poultry, eggs, dairy products, farmed fishes | Cross contamination with animals, food and humans, water
35
What are the symptoms of salmonella spp. infection?
6-48 hours after ingestion nausea, vomiting and diarrhea occur, usually self-limiting
36
What must be done with food handlers when they have a salmonella spp. infection?
Excluded from work until 3 fecal specimens are negative | May be excreted in feces for several weeks post infection
37
What are the symptoms of enteric fever?
Initial: Headache, fever, abdominal tenderness, constipation | Diarrheal stage: Gallbladder and Peyer's patches
38
How does salmonellosis colonize in the body?
Hides in a vacuole in the host cell, divides, then hides in monocytes to travel in blood stream and cause systemic infection Chronic colonization
39
How do we diagnose salmonellosis?
Recover from blood and stools
40
Where does salmonellosis colonize chronically?
In the gallbladder and biliary tree with no symptoms but still constantly shedding (Typhoid Mary)
41
What is the most common cause of bacterial gastroenteritis?
Campylobacter High ID50 Heat sensitive, invasive
42
What are the symptoms of campylobacter infection?
Lasts 2-5 days Diarrhea with blood and pus, painful (2-3 days) Abdominal pain lasting longer Self-limiting
43
Where does campylobacter come from?
Poultry, contaminated meat, water and unpasteurized milk
44
How is campylobacter identified?
By the S-shaped cells under the microscope
45
How is campylobacter treated?
Using fluoroquinolone and macrolides
46
What does vibrio cause?
Cholera (rapid dehydration by rice water stools), only infects humans
47
Where is vibrio in endemic?
Southeast Asia, parts of south america and africa
48
Where does vibrio come from?
Water environments, fish, shellfish
49
What are rice water stools?
Stools free of RBCs and WBCs, pretty much just water | Diagnostic tool
50
What is the pathogenesis of vibrio?
Mostly due to toxins that it only produces in the human gut (AB subunit, activating adenylate cyclase)
51
What is vibrio sensitive to?
Stomach acid, need very very high number of cells to get sick
52
What are the subsets of Shigella spp.?
S. sonnet (mild, most common in Canada) S. flexneri S. dysenteriae (most serious) S. boydii
53
What is the ID50 of shigellosis?
Very low (
54
What toxins does shigella spp. produce?
``` Shiga toxin (similar to E.coli 0157) Cytotoxic, enterotoxin, nerotoxic ```
55
What is the pathogenesis of shigella spp.?
Enters an epithelial cell of the intestinal tract, multiplies inside, invades neighbouring cells. When released, epithelial cell is killed, forming an access Kind of like salmonella
56
What is a complication of shigellosis?
Damage to the epithelial and kidney cells causing HUS
57
How can shigellosis be treated?
Mild is treated by rehydration | Severe needs antibiotics
58
What is clostridium difficile?
A broad spectrum antibiotic-associated diarrhea (antibiotic resistant, when other microflora are killed, it takes over) Most common cause of hospital acquired diarrhea Spore formers, toxins
59
What does clostridium difficile cause?
Mild-watery diarrhea to life-threatening toxic megacolon (surgical intervention) Pseudomembranes forming pseudomembranous colitis (fibrin, neutrophils, mucin, cellular debris)
60
What toxins does clostridium difficile produce?
Ted A (toxin A) and Ted B (toxin B) encoded by pathogenicity locus on chromosome together with negative and positive regulators of their expression
61
What is the emergent strain of clostridium difficile?
C.difficile 027 produces more TedA and B due to deletion in regulatory gene (tcdC) that down regulates the production of two toxins
62
How is clostridium difficile treated?
``` Antibiotics for a serious infection Fecal transplant (successful, rejection rate due to genetic and gender link, need someone who hasn't been on antibiotics in 5 years, stomach acid is a problem) ```
63
Does clostridium difficile ever go away?
Infection persists forever, most people never get their normal microflora back
64
What are some common causative agents for food poisoning?
Staph aureus enterotoxin (8 types, heat stable, enzyme resistant), clostridium botulinum toxin
65
How do S. aureus enterotoxins work?
``` It is a super antigen that binds to MHC class II molecules and cause T-cell stimulation Body's reaction is much more aggressive ```
66
What are the side effects of S. aureus enterotoxins?
Affects CNS, severe vomiting 3-6 hours after consumption, no diarrhea, complete recovery in 24 hours
67
Where is listeria monocytogenes found?
Animals, the environment, undercooked food, unpasteurized food, soft cheese
68
Who has an enhanced risk for listeriosis?
Pregnant women (can cross placenta) and immunocompromised individuals
69
What is the ID50 of listeria monocytogenes?
70
Is listeria monocytogenes susceptible to heat?
Yes, but survives and grows very well at room temperature (multiplies at 4 degrees)
71
How does the virulence of listeria monocytogenes work?
Gets inside cells via endocytosis, forms actin tail and spreads from cell to cell via endocytosis without ever leaving host cells Survives on macrophages
72
What are the most common cause of gastroenteritis and diarrhea?
Viruses (rotavirus, norovirus), specific to human | Impact nutritional status and growth if contracted at young age
73
What are rotaviruses?
Lt wheel naked viruses spread by oral-decal transmission
74
What are the symptoms of rotavirus infection?
Vomiting, diarrhea (very high numbers-contagious), fever | Only 6-7 days
75
How is rotavirus infection treated?
Fluid and salt replacement | Use clean, uncontaminated water
76
How can rotavirus be prevented?
Using a vaccination
77
What is a norovirus? Where does it commonly cause infection?
Calcivirus family, most common cause of food illness outbreaks Schools, nursing homes, families, cruise ships
78
What is the incubation period and rate of infection for norovirus?
24-48 hours | 50% rate of infection (highly infectious)
79
How can we determine if it is norovirus?
Unculturable so use an electron microscope or RT-PCR
80
What is the 2nd largest cause of mortality and morbidity in the world?
GI tract infections

Mechanisms of Microbial Disease (17 decks)

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